The p53 tumor suppressor gene encodes a transcription factor that contributes to several cellular activities that include apoptosis, transient growth arrest, and sustained growth arrest or senescence (1). Mutations within the p53 gene are found in about half of all human cancers (2). In cells that are functioning normally the MDM2 protein binds to p53 and maintains p53 at low levels by increasing its susceptibility to proteolysis by the 26S proteosome (3). A cell that undergoes stress loses the ability of MDM2 to bind to p53 and as a result p53 levels increase which then leads to cell cycle arrest or apoptosis (3&4). p53 induced cell cycle arrest or apoptosis can be achieved through transcriptional regulation of several genes including the cell cycle inhibitor p21, DNA repair gene GADD45, and the apoptotic inducer Bax (5). Besides MDM2 inactivation, p53 can also be functionally inactivated by mutation or binding to DNA tumor virus encoded proteins, such as SV40 large T antigen, Adenovirus E1B and papilloma virus E6 proteins (6).